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Vernix Caseosa: Formation and Functions

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Vernix Caseosa: Formation and Functions Newborn & Infant Nursing Reviews 14 (2014) 142–146 Contents lists available at ScienceDirect Newborn & Infant Nursing Reviews journal homepage: www.nainr.com Vernix Caseosa: Formation and Functions Marty Visscher, PhD a,c,⁎, Vivek Narendran, MD, MRCP, MBA b,d a Skin Sciences Program, Cincinnati Children’s Hospital Medical Center, College of Medicine, University of Cincinnati, Cincinnati, OH b Perinatal Institute, Cincinnati Children’s Hospital Medical Center, College of Medicine, University of Cincinnati, Cincinnati, OH c Department of Surgery, College of Medicine, University of Cincinnati, Cincinnati, OH d Department of Pediatrics, College of Medicine, University of Cincinnati, Cincinnati, OH article info abstract Keywords: Native vernix is a multifunctional skin cream with properties of skin moisturization/hydration, anti-infective, skin Neonatal skin cleansing, skin barrier repair, wound healing, and skin barrier protection against irritants. Vernix facilitates forma- Vernix caseosa tion of the stratum corneum (SC) in utero through yet to be fully determined mechanisms. It enables development Skin barrier of the SC barrier in the normal, full term infant through a variety of protective and adaptive mechanisms. The find- Epidermis ings provide support for the practice keeping vernix on the skin at birth and waiting at least six hours prior to bath- Stratum corneum ing newborn infants. © 2014 Elsevier Inc. All rights reserved. The skin of a healthy, full term newborn infant is well-formed, so- Lipids phisticated and highly effective at performing multiple protective func- tions at birth. The epidermis is thick and the transepidermal water loss The lipid component of vernix comprises free lipids including tri- (TEWL) is very low, equal to or lower than adults.1,2 This is remarkable glycerides, fatty acids, ceramides, cholesterol, sterol esters, wax esters, given that the developing fetus is exposed to water and amniotic fluid dihydroxy wax esters, squalene, diacylglycerol, monoacylglycerol and for nine months. Normally, long term water exposure causes skin mac- phospholipids, as well as others bound to the cell envelope.6,7 The eration, disruption of the well-organized stratum corneum (SC) struc- most abundant species are nonpolar lipids and cholesterol, ceramides ture and injury to the epidermis.3 Superficial wounds, e.g., abrasions, and free fatty acids together comprise 10%. This contrasts to the stratum involve full or partial loss of the SC. Normally, air exposure triggers the corneum lipids where cholesterol, ceramides and free fatty acids are healing process and new SC forms to cover the epidermis. If the epider- 80% of the total lipids. The most abundant monounsaturated fatty acid mis is covered with water, the SC does not form. The question is this: and C18:2n-6 is the highest polyunsaturated fatty acid.7 Branched how does an effective, well-structured skin barrier form while the infant chains are 29% of the fatty acids and include 30 different chain lengths.8 is in water? Proteins Vernix Composition Over two hundred proteins have been identified in vernix.9 The most abundant protein types were: hydrolases (14.4%), proteases Structure (10.8%), enzyme modulators (10.8%), cytoskeletal proteins (9.8%), structural proteins (6.9%), transfer/carrier proteins (5.6%), calcium- The major component of native vernix is water, at 80%, 10% protein binding proteins (5.6%), immunity proteins (5.6%) and signaling mole- and 10% lipids. This is surprising since the consistency of vernix is that of cules (4.9%). The SC proteins keratin 1, 10, 11, involucrin and filaggrin, a thick cream, usually low in water content. The water in vernix is asso- present in the stratum corneum, were also found in vernix.10,11 Free ciated with cells that are covered with an amorphous mixture of lipids, amino acids (FAA), components of natural moisturizing factor (NMF), as shown in Fig. 1.4 The cells are flattened corneocytes, about 1–2 μm were identified. Glutamic acid and histidine were higher and glycine thick, without distinct nuclei, i.e., that would be characteristic of living and serine lower than would be expected from the degradation of cells. The keratin levels are lower than fully mature stratum filaggrin, suggesting that vernix contains other sources of amino acids.12 corneum cells, vary in stage of keratinization and there are no visi- ble desmosomes.4,5 Vernix Formation During Gestation ⁎ Last Trimester Corresponding author at: Skin Sciences Program, Division of Plastic Surgery, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229 USA. Tel.: +1 513 803 0934; fax: +1 513 636 7182. Vernix has been noted around on the eyebrows of the developing E-mail address: [email protected] (M. Visscher). fetus at gestational week seventeen. As gestation continues, vernix http://dx.doi.org/10.1053/j.nainr.2014.10.005 1527-3369/© 2014 Elsevier Inc. All rights reserved. M. Visscher, V. Narendran / Newborn & Infant Nursing Reviews 14 (2014) 142–146 143 Fig. 1. Vernix structure with cells and lipids. The major component of native vernix is water at 80% by weight, 10% protein, and 10% lipids. This figure is vernix at high magnification. Note that the cells are close together and appear to be stacked. The water in vernix is associated with the cells, contained within them like “packets of water”. The cells are covered with an amorphous mixture of lipids. The cells are flattened corneocytes, about 1–2 μm thick, without distinct nuclei, i.e., that would be characteristic of living cells. The asterisks in the second picture show cells covered with lipids. starts to cover the fetal skin surface progressing from head to toe and like axis14 and this may also play a role in vernix formation as some of back to front.13 Maternal and placental hormones are believed to con- the vernix lipids are of the types produced by the sebaceous glands.6,15 trol vernix formation and coverage. One possibility is that placental or The cells in vernix may originate from the hair follicles.16 This suggests a hypothalamic corticotropic-releasing factors (CRF) signal the pituitary mechanism whereby vernix is “extruded” or squeezed out through the gland to release adrenocorticotropic hormone (ACTH), in turn causing hair shaft, onto the skin surface around the hair, eventually spreading the adrenal gland to synthesize and release androgenic steroids. Next, over the entire surface as “vernix production” continues throughout these steroids become active androgens and function within the seba- gestation (Fig. 2).17 Films of vernix (i.e., spread onto a porous substrate) ceous gland. The hair follicle has local hypothalamic-pituitary-adrenal- are hydrophobic, due to the lipids which coat the hydrated cells.18 This Fig. 2. A, B, C. Vernix formation. The fetus is bathed in amniotic fluid for nine months, yet the infant is born with a well-developed stratum corneum barrier. Panel A shows the epidermis without any stratum corneum. Maternal and placental hormones are believed to control vernix formation and coverage. Some of the vernix lipids are of the types produced by the seba- ceous glands. The cells in vernix may originate from the hair follicles. This suggests a mechanism whereby vernix is “extruded” or squeezed out through the hair shaft, onto the skin surface around the hair eventually spreading over the entire surface as “vernix production” continues throughout gestation (B). Shortly before birth, the vernix begins to detach from the skin surface under the influence of pulmonary surfactant secreted by the lung. In full term infants, the stratum corneum has formed, presumably beneath the layer of vernix (C). Download English Version: https://daneshyari.com/en/article/2673180 Download Persian Version: https://daneshyari.com/article/2673180 Daneshyari.com.
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